Journal of periodontal research最新文献

Aim: X-linked Hypophosphatemia (XLH), caused by PHEX mutations, hinders skeletal and dental mineralization and contributes to tooth loss. While XLH is associated with dental implant-related complications, no clinical or preclinical studies have investigated socket healing. XLH secondarily disrupts local mineral metabolism by increasing levels of the mineralization inhibitors, osteopontin (OPN) and inorganic pyrophosphate (PP_i). Tissue-nonspecific alkaline phosphatase (TNAP) promotes mineralization by dephosphorylating OPN and hydrolyzing PP_i. In this proof-of-principle study, we hypothesized that alveolar bone socket healing defects in the Hyp mouse model of XLH would be improved by exogenous TNAP.

Methods: Maxillary first molars were extracted from wild-type (WT) and Hyp mice at 6 weeks, and collagen gel ± mineral-targeted TNAP (TNAP-Fc-D₁₀; asfotase alfa) was placed in sockets. Submucosal injections of TNAP-Fc-D₁₀ or saline were delivered at 7 and 14 days post-procedure (dpp) in some mice. Maxillae were collected at 21 dpp for micro-computed tomography, histology, and RT-qPCR.

Results: Untreated Hyp mice showed impaired socket healing compared to WT mice in bone volume and density. TNAP delivered at the time of extraction was unable to improve healing in Hyp mice. However, additional local TNAP delivery increased both alveolar bone volume and density in Hyp mice. Histology indicated repeated TNAP increased both woven and mature bone in Hyp mouse sockets. Immunostaining for osteopontin and bone sialoprotein suggested partial resolution of osteoid accumulation.

Conclusion: TNAP enhanced socket healing in Hyp mice, overcoming inherent bone healing defects in XLH. These results provide new insights into bone healing with implications beyond alveolar bone in XLH.

Aim: This study aims to investigate the effect of inflammation on the senescence phenotype and osteogenic capacity of aged periodontal ligament cells (PDLCs), and to explore the regulatory role of the NF-κB signalling pathway in the osteogenesis of aged PDLCs.

Methods: Human PDLCs were isolated, and two ageing models were used: replicative senescence and etoposide treatment. The proliferation and migration of PDLCs were tested with the cell counting kit-8 assay, 5-ethynyl-2'-deoxyuridine staining, and scratch test. Proinflammatory cytokine levels were tested using enzyme-linked immunosorbent assay and real time-quantitative polymerase chain reaction. Osteogenic differentiation was evaluated through alkaline phosphatase activity, Alizarin Red S staining, and calcium quantification. Expression levels of nuclear factor kappa-B (NF-κB) and c-JUN pathway-related proteins were analyzed through Western blotting.

Results: Inflammatory stimulation enhanced the senescence phenotype in both young and aged PDLCs and inhibited osteogenic differentiation in aged PDLCs. During cellular ageing, NF-κB signalling downregulated the osteogenic differentiation of PDLCs by suppressing forkhead box O3a (FOXO3a) and c-JUN. Conversely, under exogenous inflammatory stimulation, NF-κB signalling inhibited osteogenesis by promoting FOXO3a phosphorylation and increasing c-JUN expression, with p21 exerting a synergistic inhibitory effect on osteogenic differentiation in aged PDLCs.

Conclusion: Inflammation aggravates cellular senescence and suppresses osteogenic differentiation in aged PDLCs through the NF-κB/FOXO3a/c-JUN signalling pathway.

Peri-implant diseases (PIDs) are highly prevalent and threaten both the success and longevity of implant-supported prostheses. Their prevention should begin before implant surgery (i.e., primordial prevention) by avoiding risk factor exposure and ensuring optimal implant placement conditions. Prehabilitation, a multimodal strategy already used in other surgical fields, can be applied to implant dentistry to optimize patient status before surgery. By addressing modifiable behavioral risk factors and strengthening systemic and local conditions, prehabilitation would enhance both short- and long-term outcomes of implant-supported rehabilitation.

This study identifies autophagy-pyroptosis crosstalk as a driver of periodontal pathogenesis and suggests ATG7 as a preliminary, context-dependent modulator.

The periodontium is a uniquely dynamic tissue system requiring precise signaling for lifelong adaptation. The canonical Wnt/β-catenin pathway is a master regulator of bone homeostasis; however, its role in the specialized environment of the alveolar bone-marked by rapid turnover, complex mechanical forces, and exposure to the oral microbiome-remains incompletely understood, particularly in the context of aging. This review critically synthesizes evidence on Wnt signaling in alveolar bone remodeling, with a focus on age-related dysregulation, contrasting established paradigms from long bone biology with emerging oral-tissue-specific data. Wnt/β-catenin signaling is essential for periodontal homeostasis, orchestrating osteoblastogenesis and mechanotransduction. Its activity is compartment-specific within the periodontium and is potently suppressed in pathology. Key mechanisms of age-related decline include the upregulation of Wnt antagonists (e.g., sclerostin, DKK1), cellular senescence, altered FoxO-Wnt crosstalk under oxidative stress, and impaired mechanosensing. These changes converge to disrupt regenerative capacity, tipping the balance toward net alveolar bone loss. Therapeutically, sclerostin inhibition demonstrates robust preclinical efficacy in rescuing bone loss in models of periodontitis and estrogen deficiency. However, the potential cardiovascular risks of systemic Wnt activation suggest that redirecting efforts toward localized delivery strategies could be a promising alternative. Aging induces a multifaceted suppression of regenerative Wnt signaling in the periodontium. Modulating the Wnt pathway shows great potential for oral bone regeneration. However, significant challenges exist, especially in designing local delivery systems that are both safe and effective. Overcoming these hurdles is crucial for successful clinical applications. Future research must bridge the gap between skeletal biology and direct oral-specific investigations to enable targeted therapies that preserve periodontal health in an aging population.

Aim: To assess the prevalence of peri-implant diseases and buccal peri-implant soft-tissue dehiscence (PISTD) and to identify the associated risk indicators.

Methods: Patients previously rehabilitated with implant-supported rehabilitations at the University of Turin Dental School were specifically recalled with a registry-based approach for this cross-sectional study. Data collection included medical and dental history, full-mouth clinical examination, and periapical radiographs. Moderate/severe peri-implantitis was diagnosed based on bone loss (direct criterion, when available) or bone level (indirect criterion) ≥ 2 mm and the presence of bleeding/suppuration. PISTD was defined as mucosal dehiscence on the buccal aspect of at least one implant site. Multilevel, multivariable logistic regression models were applied to identify factors associated with moderate/severe peri-implantitis and buccal PISTD.

Results: Of the 397 patients contacted, 146 were included (mean age 61.1 ± 14.5 years; current smokers 34.3%; stage III-IV periodontitis 65.1%) with a total of 511 dental implants (mean function time: 13.3 years [2-31]). Implant survival rate was 96.5%. Moderate/severe peri-implantitis was detected in 56.8% of patients and 34.7% of implants. Prevalence of buccal PISTD was 54.1% and 40.5%, respectively. Protective indicators for moderate/severe peri-implantitis included supportive peri-implant care > twice a year (OR = 0.16; 95% CI: 0.03-0.95), > 2 mm of keratinized tissue height (OR = 0.44; 95% CI: 0.21-0.95), and correct mesio-distal implant positioning (OR = 0.54; 95% CI: 0.32-0.94). Risk indicators included stage III-IV periodontitis (OR = 2.82; 95% CI: 1.30-6.15), function time ≥ 10 years (OR = 3.02; 95% CI: 1.55-5.89), bisphosphonate use during follow-up (OR = 5.96; 95% CI: 1.33-26.66), and presence of a cantilever (OR = 5.51; 95% CI: 1.56-19.38). For PISTD, protective indicators were mandibular location (OR = 0.45; 95% CI: 0.25-0.81), thick buccal soft-tissue phenotype (OR = 0.18; 95% CI: 0.08-0.42), and > 2 mm of keratinized tissue height (OR = 0.05; 95% CI: 0.02-0.15). Risk indicators included peri-implantitis (OR = 2.21; 95% CI: 1.25-3.91), use of intermediate abutments (OR = 4.92; 95% CI: 1.92-12.58), and proximity to adjacent implants (OR = 3.35; 95% CI: 1.50-7.48) or edentulous spaces (OR = 3.38; 95% CI: 1.51-7.54).

Conclusion: In this long-term, university-based cohort, peri-implant diseases and PISTD were highly prevalent. Multiple patient- and implant-level factors emerged as significant risk or protective indicators. Despite the widespread occurrence of peri-implant diseases, long-term implant survival remained high, challenging current diagnostic thresholds and underscoring the need for refined, progression-based definitions.

The present findings demonstrate that low-level laser therapy reduces postoperative pain levels associated with the palatal donor site in free gingival graft surgeries, as well as accelerating the clinical healing of the surgical wound. Low-level laser therapy is associated with improved postoperative morbidity of the donor area in free gingival graft.

Aim: To examine the impact of emulated natural tooth preservation or dental rehabilitation scenarios on diet quality among older adults in the United States, assessing what diet quality would be if people's dentition or rehabilitation status were improved.

Methods: Data from 2606 participants aged ≥ 60 across four NHANES cycles (2011-2018) were analyzed. Dentition status and prosthetic rehabilitation were clinically assessed, and diet quality was measured using the Healthy Eating Index (HEI)-2020. The modified treatment policies (MTP) framework was used to emulate hypothetical interventions of retaining natural teeth or providing prosthetic rehabilitation. Odds ratios (OR) for achieving better diet quality under each scenario were estimated using doubly robust targeted maximum likelihood estimation (TMLE).

Results: If all participants retained ≥ 25 teeth, the likelihood of achieving better HEI scores increased by 51% (OR = 1.51, 95% CI: 1.32-1.69). In a pragmatic scenario where each dentition group was shifted up by one level (edentulous → 1-9 teeth, 1-9 teeth → 10-19 teeth, 10-19 teeth → 20-25 teeth, 1-9 teeth → ≥ 25 teeth), the population had a 20% higher likelihood of achieving better diet quality (OR = 1.22, 95% CI: 1.14-1.29). Prosthetic rehabilitation yielded comparatively smaller effects, with rehabilitation in individuals with < 25 teeth improving the likelihood of better diet quality by 8% (OR = 1.08, 95% CI: 1.03-1.12).

Conclusion: The present observational study suggests that preserving natural teeth has a stronger population-level impact on diet quality than prosthetic rehabilitation replacing missing teeth in older adults.